Objective: Changes of obesity on renal perfusion and metabolism are poorly understood. Our aims were to evaluate whether obesity increases renal regional hemodynamics and metabolism in vivo, and to determine the effects of weight loss.

Methods: 23 morbidly obese and 15 age- and sex-matched nonobese controls were recruited. Renal perfusion and fatty acid uptake (FAU) were measured using PET-CT scanning and [15O]- H2O and [18F]fluoro-6-thia-heptadecanoic acid ([18F]THA), respectively. Kidney volumes and radiodensity were measured by CT and cardiac output by MRI. Intraglomerular pressure (Pglo) was estimated by Gomez formula. Obese subjects were re-studied six months after bariatric surgery.

Results: As compared to controls, obese subjects had larger renal volume (340[118] vs. 256[63] ml, median[interquartile range]) and lower renal radiodensity (15.3[13.1] vs. 31.5[9.8] units, p≤0.05 for both), suggesting accumulation of water and/or lipid. Both cardiac output and glomerular filtration rate (eGFR) were increased by ∼25% in the obese. While there were no differences in total renal perfusion between the two groups, Pglo was higher in the obese (61±5 mmHg vs. 55±3 of controls, p<0.001). In both groups, regional blood flow was 50% higher in the cortex than medulla; in either region, FAU was higher in the obese (6.3±1.8 vs. 4.1±1.5 µmol.min-1.100g-1, and 7.5±2.2 vs. 4.6±2.1, both p≤0.05), mostly as a consequence of higher plasma FFA levels. Post-surgery (weight loss = 26±8 kg), renal volume, GFR, and Pglo all decreased and renal radiodensity increased to levels similar to controls. On the contrary, cortical and medullary FAU was not normalized.

Conclusions: In obesity, renal hemodynamics are indicative of an incomplete protection against hyperperfusion and renal fatty acid uptake is increased, driven by higher substrate availability. Surgically-induced major weight loss reverses the hemodynamic but not the metabolic changes.


E. Rebelos: None. P. Dadson: None. V. Oikonen: None. H. Iida: None. J.C. Hannukainen: None. P. Iozzo: None. E. Ferrannini: None. P. Nuutila: Research Support; Self; AstraZeneca.


Academy of Finland; University of Turku; Turku University Hospital

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.